Application of modular kinetic analysis to mitochondrial oxidative phosphorylation in skeletal muscle of birds exposed to acute heat stress

We previously showed that heat stress stimulates reactive oxygen species (ROS) production in skeletal muscle mitochondria of birds, probably via an elevation in mitochondrial membrane potential (ΔΨ). To clarify the mechanism underlying the elevation of ΔΨ, modular kinetic analysis was applied to oxidative phosphorylation in skeletal muscle mitochondria of heat-stressed birds (34 °C for 12 h). In the birds exposed to heat stress, ‘substrate oxidation’ (a ΔΨ-producer) was increased compared to control (24 °C) birds, although there was little difference in ‘proton leak’ (a ΔΨ-consumer), suggesting that an elevation in the ΔΨ at state 4 may be due to enhanced substrate oxidation. It thus appears that enhanced substrate oxidation plays a crucial role in the overproduction of ROS for heat-stressed birds, probably via elevated ΔΨ.     

Enhanced lipoxygenase activity is involved in the stress response but not in the harmful lipid peroxidation and cell death of short-term cadmium-treated barley root tip

Root growth inhibition and radial root swelling were the characteristic symptoms of barley root tips after the short-term exposure of roots to 15 and 30 μM Cd. Higher Cd concentrations caused extensive cell death and root growth arrest. Enhanced lipid peroxidation was observed as early as 1 h after the short-term treatment in a Cd concentration-dependent manner. In contrast to lipid peroxidation, the induction of lipoxygenase activity was detected only 3 h after the exposure of roots to 15 or 30 μM Cd. In addition, it was not observed in 60 μM Cd-treated root tips. The highest lipoxygenase activity was detected 6 h after 15 μM Cd treatment in the meristematic and elongation zone of root tip and was probably associated with the radial expansion of cells. Our results indicate that the upregulation of lipoxygenase is an important component of stress response in barley roots to toxic Cd. It is probably involved in the morphological stress response of root tips or/and in the alleviation of Cd-induced toxic alterations in plant cell membranes, but it is not responsible for the Cd-induced harmful lipid peroxidation and cell death.     

急性低压低氧对大鼠空间学习记忆的影响及与海马内孤啡肽的关系

目的:研究暴露在不同海拔高度的急性低压低氧环境中,大鼠空间学习记忆能力的变化及与海马内孤啡肽的关系.方法:采用低压舱模拟4 500 m(中度)和7 500 m(重度)两种海拨高度,Morris水迷宫训练方法和反转录多聚酶链式反应(RT-PCR)技术.结果:①海马内孤啡肽mRNA表达在急性重度低压低氧(8 h/d,连续6 d)后明显增加,然而在Morris 水迷宫训练(6 counts/d,连续6 d,定位航行潜伏期逐渐缩短)后则显著降低.②急性低压低氧后,定位航行潜伏期明显延长,而海马内孤啡肽mRNA表达较学习记忆训练组明显升高.结论:海马内孤啡肽参与急性低压低氧降低大鼠空间学习记忆的机制.     

Preinduction of HSP70 promotes hypoxic tolerance and facilitates acclimatization to acute hypobaric hypoxia in mouse brain

It has been shown that induction of HSP70 by administration of geranylgeranylacetone (GGA) leads to protection against ischemia/reperfusion injury. The present study was performed to determine the effect of GGA on the survival of mice and on brain damage under acute hypobaric hypoxia. The data showed that the mice injected with GGA survived significantly longer than control animals (survival time of 9.55 ± 3.12 min, n = 16 vs. controls at 4.28 ± 4.29 min, n = 15, P < 0.005). Accordingly, the cellular necrosis or degeneration of the hippocampus and the cortex induced by sublethal hypoxia for 6 h could be attenuated by preinjection with GGA, especially in the CA2 and CA3 regions of the hippocampus. In addition, the activity of nitric oxide synthase (NOS) of the hippocampus and the cortex was increased after exposure to sublethal hypoxia for 6 h but could be inhibited by the preinjection of GGA. Furthermore, the expression of HSP70 was significantly increased at 1 h after GGA injection. These results suggest that administration of GGA improved survival rate and prevented acute hypoxic damage to the brain and that the underlying mechanism involved induction of HSP70 and inhibition of NOS activity.     

野牛草叶片活性氧及其清除系统对水分胁迫的响应

逆境条件下活性氧产生及其清除效率是衡量植物抗性的重要指标,而活性氧对植物组织的氧化伤害和抗氧化酶活性常因材料的遗传或生理差异性而发生变化。以同一基因型的野牛草(Buchloe dactyloides(Nutt.)Engelm'texoka')克隆分株叶片为材料,采用Hoagland营养液培养,研究了10%、20%和30%PEG-6000模拟干旱胁迫下,野牛草叶片活性氧的产生、脂质过氧化和抗氧化酶活性变化规律。结果表明:随着PEG-6000浓度的增加及胁迫时间的延长,超氧阴离子(O2-.)的产生速率、过氧化氢(H2O2)和丙二醛(MDA)含量均显著增加;超氧化物歧化酶(SOD EC1.15.1.1)、愈创木酚过氧化物酶(G-POD EC1.11.1.7)和过氧化氢酶(CATEC1.11.1.6)活性呈先上升后下降的变化趋势;SOD、G-POD与CAT活性达到峰值的时间随PEG-6000浓度的增加而提前。认为水分胁迫下,抗氧化酶可有效清除活性氧自由基,但随胁迫时间的延长,抗氧化酶活性受到抑制。     

Involvement of Reactive Oxygen Species in Plant Mitochondrial Response to Low-Temperature Stress

The review presents data for the generation of the reactive oxygen species (ROS) in mitochondria during low-temperature stress. The relation of lipid peroxidation processes in membranes to the induction of low-temperature stress is demonstrated. The data for the involvement of the mitochondrial uncoupling proteins and the processes of uncoupling oxidation and phosphorylation in the regulation of mitochondrial ROS formation during low-temperature stress are considered.     

Combined effect of vanadium(V) and chromium(III) on lipid peroxidation in liver and kidney of rats

Since chromium(III) was demonstrated to have antioxidative action, we have decided to study the effect of this element on V-induced LPO in liver and kidney of rats. Outbred 2-month-old, albino male Wistar rats received daily, for a period of 12 weeks: group I (control), deionized water to drink; group II, sodium metavanadate (SMV) solution at a concentration of 0.100mgV/mL; group III, chromium chloride (CC) solution at a concentration of 0.004mgCr/mL and group IV, SMV-CC solution at a concentration of 0.100mgV and 0.004mgCr/mL. The particular experimental groups took up with drinking water about 8.6mgV/kg b.w./24h (group II), 0.4mgCr/kg b.w./24h (group III), 9mgV and 0.36mgCr/kg b.w./24h (group IV). The V- or Cr-treated groups had higher concentrations of these two elements in liver and kidney compared to the controls. The administration of vanadium alone caused a significant decrease in fluid intake and in body weight gain compared to the controls. In liver supernatants obtained from all tested rats a statistically significant increase in MDA concentration was demonstrated in spontaneous LPO in comparison with the control rats. Moreover, in rats intoxicated with vanadium alone a statistically significant increase in liver MDA level was observed in the presence of 100microM NaVO(3). Instead, in supernatants of liver received from rats treated with chromium alone, a statistically significant increase in MDA concentration in comparison with the controls was found in the presence of 400microM NaVO(3). In kidney supernatants obtained from rats treated with chromium alone, a statistically significant increase in lipid peroxidation was shown in the presence of 30microM FeSO(4) and 400microM NaVO(3). These results show that the tested doses of vanadium(V) and chromium(III) ingested by rats with their drinking water caused significant alterations in internal organs, especially in liver. Under the conditions of our experiment, Cr(III) did not demonstrate antioxidant action, it rather had an oxidant effect.     

Bcl-2 prevents hypoxia/reoxygenation-induced cell death through suppressed generation of reactive oxygen species and upregulation of Bcl-2 proteins

The function of bcl-2 in preventing cell death is well known, but the mechanisms whereby bcl-2 functions are not well characterized. One mechanism whereby bcl-2 is thought to function is by alleviating the effects of oxidative stress upon the cell. To examine whether Bcl-2 can protect cells against oxidative injury resulting from post-hypoxic reoxygenation (H/R), we subjected rat fibroblasts Rat-1 and their bcl-2 transfectants b5 to hypoxia (5% CO2, 95% N2) followed by reoxygenation (5% CO2, 95% air). The bcl-2 transfectants exhibited the cell viability superior to that of their parent non-transfectants upon treatment with reoxygenation after 24-, 48-, or 72-h hypoxia, but not upon normoxic serum-deprivation or upon serum-supplied hypoxic treatment alone. Thus bcl-2 transfection can prevent cell death of some types, which occurred during H/R but yet not appreciably until termination of hypoxia. The time-sequential events of H/R-induced cell death were shown to be executed via (1) reactive oxygen species (ROS) production at 1-12 h after H/R, (2) activation of caspases-1 and -3, at 1-3 h and 3-6 h after H/R, respectively, and (3) loss of mitochondrial membrane potential (DeltaPsi) at 3-12 h after H/R. These cell death-associated events were prevented entirely except caspase-1 activation by bcl-2 transfection, and were preceded by Bcl-2 upregulation which was executed as early as at 0-1 h after H/R for the bcl-2 transfectants but not their non-transfected counterpart cells. Thus upregulation of Bcl-2 proteins may play a role in prevention of H/R-induced diminishment of cell viability, but may be executed not yet during hypoxia itself and be actually operated as promptly as ready to go immediately after beginning of H/R, resulting in cytoprotection through blockage of either ROS generation, caspase-3 activation, or DeltaPsi decline.     

快速脱水与复水过程中2种藓类植物的活性氧代谢与脂质过氧化特征

以来自不同水分生境的金发藓和湿地匐灯藓为材料,对二者在脱水与复水胁迫条件下的活性氧代谢、脂质过氧化损伤程度及其抗氧化系统应答的差异进行比较研究。结果显示:在脱水与复水过程中,(1)硅胶快速脱水更接近阳光直射条件下藓类植物的水分丧失。(2)随着含水量的变化,湿地匐灯藓虽然能够在复水后迅速修复细胞的完整性,但变化剧烈;金发藓则能够始终维持较低的膜透性。(3)2种藓类植物的丙二醛(MDA)含量变化均呈先升后降趋势,但金发藓的MDA含量明显低于湿地匐灯藓。(4)2种藓类植物的超氧阴离子自由基(O2.-)产生速率和过氧化氢含量(H2O2)的变化均与MDA含量变化相似,且金发藓活性氧水平明显高于湿地匐灯藓。(5)2种藓类植物的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和抗坏血酸过氧化物酶(APX)活性受活性氧诱导亦呈先升后降的趋势,但金发藓抗氧化酶对活性氧迸发的应答更快,活性更强。(6)2种藓类植物的抗坏血酸(AsA)含量呈先降后升态势,但金发藓的含量低于湿地匐灯藓。研究表明,来自不同生境的2种藓类植物对脱水胁迫所致的氧化胁迫均具有很强的适应能力,尤其是复水过程中的修复能力,但不同藓类可能通过不同途径和机制来适应脱水所致的氧化胁迫;来自易发生水分亏缺生境的金发藓可能因具有更强抗氧化能力,从而获得比来自水分充沛生境的湿地匐灯藓更高的脱水耐性。     

Ontogenic profile of some antioxidants and lipid peroxidation in human placental and fetal tissues

Reactive oxygen species (ROS) pose a serious threat to maternal and fetal health during pregnancy. However, there is little information on the oxidative damage caused by ROS and its protection during prenatal life. The present study highlights the status of various antioxidants in human placental and fetal tissues at different phases of gestation. The activity profile of scavenging enzymes, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase as well as the concentrations of non-enzymatic antioxidants, ascorbic acid, -tocopherol, bilirubin and glutathione have been determined in human placental whole homogenate, placental brush border membrane and fetal liver over gestational periods ranging from 6 weeks of pregnancy till birth. The ontogenic profile of lipid peroxidation, a marker of oxidative damage has also been investigated in the feto-placental system. Catalase, superoxide dismutase and glutathione reductase activities increased significantly, but glutathione peroxidase activity remained almost the same throughout development. Except - tocopherol and bilirubin, the concentrations of other non-enzymic scavengers followed a significant increasing trend with advancement of pregnancy. Results indicate that there is gradual suppression of lipoperoxide formation with the progress of gestation to protect the fetus against oxygen toxicity.     

Natural and synthetic antioxidants: An updated overview

Abstract

The current understanding of the complex role of ROS in the organism and pathological sequelae of oxidative stress points to the necessity of comprehensive studies of antioxidant reactivities and interactions with cellular constituents. Studies of antioxidants performed within the COST B-35 action has concerned the search for new natural antioxidants, synthesis of new antioxidant compounds and evaluation and elucidation of mechanisms of action of both natural and synthetic antioxidants. Representative studies presented in the review concern antioxidant properties of various kinds of tea, the search for new antioxidants of herbal origin, modification of tocopherols and their use in combination with selenium and properties of two promising groups of synthetic antioxidants: derivatives of stobadine and derivatives of 1,4-dihydropyridine.     

Spatio-temporal relief from hypoxia and production of reactive oxygen species during bud burst in grapevine (Vitis vinifera)

Background and Aims Plants regulate cellular oxygen partial pressures (pO₂), together with reduction/oxidation (redox) state in order to manage rapid developmental transitions such as bud burst after a period of quiescence. However, our understanding of pO₂ regulation in complex meristematic organs such as buds is incomplete and, in particular, lacks spatial resolution.Methods The gradients in pO₂ from the outer scales to the primary meristem complex were measured in grapevine (Vitis vinifera) buds, together with respiratory CO₂ production rates and the accumulation of superoxide and hydrogen peroxide, from ecodormancy through the first 72 h preceding bud burst, triggered by the transition from low to ambient temperatures.Key Results Steep internal pO₂ gradients were measured in dormant buds with values as low as 2·5 kPa found in the core of the bud prior to bud burst. Respiratory CO₂ production rates increased soon after the transition from low to ambient temperatures and the bud tissues gradually became oxygenated in a patterned process. Within 3 h of the transition to ambient temperatures, superoxide accumulation was observed in the cambial meristem, co-localizing with lignified cellulose associated with pro-vascular tissues. Thereafter, superoxide accumulated in other areas subtending the apical meristem complex, in the absence of significant hydrogen peroxide accumulation, except in the cambial meristem. By 72 h, the internal pO₂ gradient showed a biphasic profile, where the minimum pO₂ was external to the core of the bud complex.Conclusions Spatial and temporal control of the tissue oxygen environment occurs within quiescent buds, and the transition from quiescence to bud burst is accompanied by a regulated relaxation of the hypoxic state and accumulation of reactive oxygen species within the developing cambium and vascular tissues of the heterotrophic grapevine buds.     

低氧应激下甘肃鼢鼠与SD 大鼠心脏抗氧化酶和ATP 酶活性的比较

为探讨低氧应激下甘肃鼢鼠心脏对抗氧化损伤和电生理紊乱的可能机制,对甘肃鼢鼠和SD 大鼠在4. 5%氧浓度下分别进行2 h、4 h、6 h、8 h、10 h、16 h 低氧应激,比较常氧和各时程低氧下二者心脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)和Ca^{2 +} - ATP 酶、Ca^{2 +} - Mg^{2 +} - ATP 酶、Na ⁺ - K ⁺ - ATP酶活性,以丙二醛(MDA)含量作为机体氧化损伤指标。结果显示,常氧组甘肃鼢鼠GR 活性比SD 大鼠高,SOD、CAT、Ca^{2 +}-ATP 酶、Ca^{2 +} - Mg^{2 +} - ATP 酶和Na ⁺ - K ⁺ - ATP 酶活性及MDA 含量与SD 大鼠相比均无显著性差
异;低氧组甘肃鼢鼠SOD、CAT、GR、Ca^{2 +} - ATP 酶、Ca^{2 +} - Mg^{2 +} - ATP 酶和Na ⁺ - K ⁺ - ATP 酶活性迅速升高,显著高于SD 大鼠,MDA 含量则显著低于SD 大鼠。说明甘肃鼢鼠心脏通过提高抗氧化酶活性清除低氧诱导产生的多余自由基,并通过提高ATP 酶活性保证心电活动正常、心率稳定,应对低氧应激。     

Aluminium-induced production of oxygen radicals, lipid peroxidation and DNA damage in seedlings of rice (Oryza sativa)

The effect of aluminium (Al) on seedlings of two rice cultivars, Pusa Basmati and Vikas was investigated after different hours of exposure to 80 mol/L of external Al supply. With increasing time of exposure, the growing seedlings readily absorbed Al and its localization was greater in roots than shoots. Prolonged exposure to Al intensified lipid peroxidation, changed the activities of SOD and peroxidase and caused DNA damage. However, differential responses were observed between the seedlings of two rice cultivars under Al stress. A close inverse relationship existed between decreased root growth and increased Al accumulation, lipid peroxidation, SOD, peroxidase activities and DNA damage. The results demonstrate that roots are the major sites of Al localization and accumulation of Al promoted oxygen free radicals mediated peroxidation of membranes as evidenced by increased MDA levels and the activities of SOD and peroxidase. Our results for the first time showed that Al can cause DNA damage in rice.     

The relation between sphingomyelinase activity, lipid peroxide oxidation and NO-releasing in mice liver and brain

We used animal models to study connection between oxidating system and sphingomyelin signaling cascade, because this models are more close related to people disease. Activation of n-sphingomyelinase (n-SMase) in mice liver and brain is coincided in time with increased level of peroxide products (conjugated dienes) after injection of tumor necrosis factor alpha (TNF-alpha). We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF-alpha in animal organs. Nitric oxide (NO) donors (S-nitrosoglutathione and dinitrosyl iron complex) reversibly inhibited activity of n-SMase and decreased level of lipid peroxidation products. This data proposed that both SMase and messengers of oxidative systems could be targets for NO-derived oxidants.